The Therapeutic Potential of Poly(ADP-Ribose) Polymerase Inhibitors
By László Virág, C. Szabó. Pharmacological Reviews, 2002
1,416 citations recorded by the source corpus.
Subfields: Cardiology and Cardiovascular Medicine, Complementary and alternative medicine, Oncology
View Paper: https://www.semanticscholar.org/paper/a9b6cf1403318230441a2b510200bd9ade0d82ff
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In Cardiology and Cardiovascular Medicine
In Complementary and alternative medicine
In Oncology
Citations in the corpus
- Poly(ADP-ribose) polymerase and the therapeutic effects of its inhibitors (2005, methodology): “Design, synthesis, and evaluation of 3,4-dihydro-2H-[1,4]diazepino[6,7,1-hi]indol-1-ones as inhibitors of poly(ADP-ribose) polymerase.”
- REACTIVE OXYGEN SPECIES, CELLULAR REDOX SYSTEMS AND APOPTOSIS (2010, positive): “For instance, NADH/NAD+ was shown to modulate gene transcription via the carboxy-terminal binding protein (CtBP) [47], Ca2+ signaling via cyclic ADP-ribose [48], cell death via poly (ADP-ribose) polymerase-1 (PARP) [49] and sirtuin protein function (see section 2.3.2).”
- Nicotinamide and PNC1 govern lifespan extension by calorie restriction in Saccharomyces cerevisiae (2003, background): “Moreover, the poly(ADP-ribose) polymerase family of proteins, which are involved in many processes including DNA repair, telomere-length regulation and the opening of chromatin associated with stress-activated genes, are also inhibited by nicotinamid”
- Computational design of receptor and sensor proteins with novel functions (2003, background): “The TNT.R3 receptor represents a first step in the development of reagentless fluorescent sensors to detect the source of underwater TNT plumes that leach into the sea from unexploded ordnance in coastal waters, using plume-tracing underwater robotic vehicles 27 .”
- Peroxynitrite: biochemistry, pathophysiology and development of therapeutics (2007, background): “Amplification of peroxynitrite-mediated mitochondrial toxicity may also involve amplification mechanisms involving extramitochondrial pathways, including the nuclear enzyme poly(ADP-ribose) polymerase (PARP”
- Mechanisms of neuronal cell death in ischemic stroke and their therapeutic implications (2021, background): “NAD is a substrate for PARP‐1, and when DNA damage occurs, PARP1 is promoted to bind acceptor proteins (hetero‐modification) or PARP1 itself (automodification).(297,298) AIF then binds to the PARP1 polymer, inducing AIF release from mitochondria.”
- NAD+/NADH and NADP+/NADPH in Cellular Functions and Cell Death: Regulation and Biological Consequences (2008, neutral): “cycle progression (296), many studies have been conducted to”
- The role of oxidative stress during inflammatory processes (2013, background): “…enzymatic inhibitors targeting NADPH oxidase (Drummond et al., 2011), NO synthase (Feihl et al., 2004), xanthine oxidase (Pacher et al., 2006), or PARP (Virag and Szabo, 2002), as well as catalytic antioxidants, including superoxide dismutase mimetics (Muscoli et al., 2003) and peroxynitrite…”
- ABT-888, an Orally Active Poly(ADP-Ribose) Polymerase Inhibitor that Potentiates DNA-Damaging Agents in Preclinical Tumor Models (2007, background): “Whereas PARP is ubiquitously expressed in almost all types of eukaryotic cells (9), PARP activity is increased in the nuclei of actively proliferating cells (1).”